ReviewCardiovascular endocrinology & metabolism2025
Insulin resistance spawns hypertriglyceridemia-induced acute pancreatitis and diabetic ketoacidosis: an evolving metabolic cascade.
Review in Cardiovascular endocrinology & metabolism, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.
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Who cites it
6 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Evaluating the efficacy of intensified insulin therapy in hypertriglyceridemic acute pancreatitis management: a systematic review and meta-analysis.Frontiers in medicine · 2026Pooled it
- The triglyceride-glucose index modulates the association between diabetes duration and insulin resistance in type 2 diabetes: a large cross-sectional study.Frontiers in endocrinology · 2026Trial
- The Correlation Analysis of C-Reactive Protein-Triglyceride-Glucose Index with the Severity of Hyperlipidemic Acute Pancreatitis.Digestive diseases and sciences · 2026Article
- Incidence and Predictors of Acute Pancreatitis in Patients With Diabetic Ketoacidosis (DKA) and Hyperosmolar Hyperglycemic State (HHS): A Multicenter Retrospective Study.Endocrine practice : official journal of the American College of Endocrinology and the American Association of Clinical Endocrinologists · 2026Article
- Differences in clinical features and prognosis between hypertriglyceridemia and other causes of acute pancreatitis: a dual perspective based on metabolic disorders and inflammatory response.Frontiers in endocrinology · 2026Article
- C-reactive protein-triglyceride-glucose index predicts acute pancreatitis severity: a retrospective cross-sectional study.Frontiers in endocrinology · 2026Article
Corrections and comments
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Insulin resistance (IR) is associated with uncontrolled lipolysis, leading to the release of free fatty acids, ectopic fat accumulation, and hypertriglyceridemia (HTG). Adipose IR is the primary factor contributing to severe HTG, which interacts with deregulated hepatic IR (Hep-IR), resulting in hypertriglyceridemic acute pancreatitis (HTGAP) and diabetic ketoacidosis (DKA). This differs from the traditional concept of 'metabolic syndrome', and demonstrates a developing metabolic cascade triggered by adipose IR that fosters pathological changes, creating a self-perpetuating cycle and establishing a two-way feedback loop with Hep-IR. This loop leads to lipotoxicity, causing self-hydrolysis of the pancreas and ultimately resulting in HTGAP. Severe HTG and HTGAP prompt the release of counter-regulatory hormones that exacerbate hyperglycemia and lipolysis, initiating a downward spiral from HTGAP to DKA.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.